Erratum in

Abstract

Placenta-specific protein 1 (Plac1), which is selectively expressed in the placental syncytiotrophoblast in adult normal tissues, plays an essential role in normal placental and embryonic development. Accumulating evidence suggests that enhanced Plac1 expression is closely associated with the progression of human cancer. Whether Plac1 contributes to the pathophysiology of hepatocellular carcinoma (HCC) remains unclear. In the present study, our data revealed that the expression of Plac1 in human HCC tissues was upregulated, which significantly correlated with metastasis of HCC. Knockdown of Plac1 by small interfering RNA (siRNA) in Bel-7402 and HepG2 cells resulted in decreasing tumor cell proliferation and increasing apoptosis, which implied the oncogenic potential of Plac1. Moreover, silencing of Plac1 induced G1 cell cycle arrest through suppression of cyclin D1 and CDK4 expression. Furthermore, depletion of Plac1 repressed epithelial-mesenchymal transition (EMT), with decreased cell migration and invasion, supporting upregulated E-cadherin expression and downregulated vimentin, twist and snail expression that characterize EMT. Further study suggested that decreased Plac1 expression attenuated the phosphorylation of Akt. These findings have uncovered that Plac1 plays a pivotal role in the progression of HCC, and may serve as a novel therapeutic target for HCC.